One stage in the palatal fusion process is epithelial autolysis. One objective of this proposal is to probe the mechanism underlying this event. To accomplish this, I propose to study those cellular changes brought about by the drug hadacidin. Previous studies have shown that this teratogen blocks the de novo synthesis of AMP by inhibiting the enzyme adenylosuccinate synthetase. We have shown that the eukaryotic microorganism Dictyostelium discoideum contains this enzymic activity and that its level declines with the onset of cellular differentiation. Further we have shown that hadacidin also causes changes to certain physiological functions such as osmotic stability and nutrient transport. We plan to continue our investigations on the effects of hadacindin on properties of the cell surface. We also plan to follow the fate of hadacidin after it is taken up by the cells as well as to purify further the adenylosuccinate synthetase of this organism.